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SUMMARY Prostacyclin is the principal product of prostaglandin (PG) endoperoxide (PGH,) metabolism in rabbit mesenteric arteries and veins, as assessed by synthesis of 6-oxo-PGFla. Formation of PGE, PGD, PGFfc, and C17-hydroxyacid of PGH, (HHT) were also detected but arose probably from non-enzymic decomposition of PGH,. The effects of prostacyclin (PGI,), 6-oxo-PGFla and PGE, on sympathetic nerre function have been studied, using rabbit mesenteric arteries and veins in vitro. In mesenteric arterial strips, prostacyclin, when administered or when synthesized endogenously, attenuates contractions caused by electrical field stimulation of intramural nerves by reducing arterial responsiveness to the released norepinephrine. In veins, prostacyclin also diminishes output of the transmitter. In arteries and veins, 6-OXO-PGFK, did not affect the output of transmitter or the contractions induced by exogenous norepinephrine. In arteries and veins, PGE, inhibited the output of adrenergic transmitter caused by nerve stimulation and was more active than prostacyclin. In arteries, PGE, reduced the contractions caused by added norepinephrine but in veins, PGE, augmented the effects. Thus, in mesenteric arteries and veins of rabbits, endogenous prostacyclin could normally act to oppose sympathetic nerve function. The predominant action in arteries is to attenuate smooth muscle responsiveness to the released transmitter, rather than to reduce adrenergic transmitter output. In veins, dulling of nerve function could additionally be brought about by a reduction in transmitter release.

Effects of prostacyclin (PGI2), 6-oxo-PGF1 alpha and PGE2 on sympathetic nerve function in mesenteric arteries and veins of the rabbit in vitro.